Prolactin inhibits oestrogen synthesis in the ovary.
In 20% of cases of secondary amenorrhoea, hyperprolactinaemia prevents ovulation by impairing normal follicular development, but little is known of the biochemical basis for this effect. Bromocriptine can restore follicular growth and ovulation by inhibiting the release of prolactin from the pituitary. The suckling stimulus causes an increase in prolactin levels, and ovarian follicles fail to develop fully, thus inducing an anovulatory state throughout lactation in many mammals. We report here experiments with cultured granulosa cells which suggest that this contraceptive action of prolactin is due to its ability to interfere with the action of follicle-stimulating hormone (FSH) on the synthesis of oestrogen.
D000818:Animals; D001141:Aromatase / Q000378:metabolism; D002478:Cells, Cultured; D004967:Estrogens / Q000096:biosynthesis*; D005260:Female; D005640:Follicle Stimulating Hormone / Q000037:antagonists & inhibitors; D006107:Granulosa Cells / Q000378:metabolism; D010053:Ovary / Q000378:metabolism*; D010060:Ovulation / Q000187:drug effects; D011388:Prolactin / Q000494:pharmacology*; D051381:Rats; D013739:Testosterone / Q000378:metabolism
D004967:Estrogens; D013739:Testosterone; D011388:Prolactin; D005640:Follicle Stimulating Hormone; D001141:Aromatase